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dc.contributor.author
Holschneider, Daniel P.
dc.contributor.author
Guo, Yumei
dc.contributor.author
Wang, Zhuo
dc.contributor.author
Roch, Margareth
dc.contributor.author
Scremin, Oscar Umberto
dc.date.available
2017-07-28T20:24:12Z
dc.date.issued
2013-01
dc.identifier.citation
Holschneider, Daniel P.; Guo, Yumei; Wang, Zhuo; Roch, Margareth; Scremin, Oscar Umberto; Remote brain network changes after unilateral cortical impact injury and their modulation by Acetylcholinesterase inhibition; Mary Ann Liebert Inc; Journal of Neurotrauma; 30; 11; 1-2013; 907-919
dc.identifier.issn
0897-7151
dc.identifier.uri
http://hdl.handle.net/11336/21589
dc.description.abstract
We explored whether cerebral cortical impact injury (CCI) effects extend beyond direct lesion sites to affect remote brain networks, and whether acetylcholinesterase (AChE) inhibition elicits discrete changes in functional activation of motor circuits following CCI. Adult male rats underwent unilateral motor-sensory CCI or sham injury. Physostigmine (AChE inhibitor) or saline were administered subcutaneously continuously via implanted minipumps (1.6 micromoles/kg/day) for 3 weeks, followed by cerebral perfusion mapping during treadmill walking using [14C]-iodoantipyrine. Quantitative autoradiographs were analyzed by statistical parametric mapping and functional connectivity (FC) analysis. CCI resulted in functional deficits in the ipsilesional basal ganglia, with increased activation contralesionally. Recruitment was also observed, especially contralesionally, of the red nucleus, superior colliculus, pedunculopontine tegmental nucleus, thalamus (ventrolateral n., central medial n.), cerebellum, and sensory cortex. FC decreased significantly within ipsi- and contralesional motor circuits and between hemispheres, but increased between midline cerebellum and select regions of the basal ganglia within each hemisphere. Physostigmine significantly increased functional brain activation in the cerebellar thalamocortical pathway (midline cerebellum/ventrolateral thalamus/motor cortex), subthalamic nucleus/zona incerta, and red nucleus and bilateral sensory cortex. In conclusion, CCI resulted in increased functional recruitment of contralesional motor cortex and bilateral subcortical motor regions, as well as recruitment of the cerebellar– thalamocortical circuit and contralesional sensory cortex. This phenomenon, augmented by physostigmine, may partially compensate motor deficits. FC decreased inter-hemispherically and in negative, but not positive, intra-hemispherical FC, and it was not affected by physostigmine. Circuit-based approaches into functional brain reorganization may inform future behavioral or molecular strategies to augment targeted neurorehabilitation.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Mary Ann Liebert Inc
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Brain Imaging
dc.subject
Brain Trauma
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Rats
dc.subject
Autoradiography
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Otros Tópicos Biológicos
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Ciencias Biológicas
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CIENCIAS NATURALES Y EXACTAS
dc.title
Remote brain network changes after unilateral cortical impact injury and their modulation by Acetylcholinesterase inhibition
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2017-07-28T18:01:18Z
dc.journal.volume
30
dc.journal.number
11
dc.journal.pagination
907-919
dc.journal.pais
Estados Unidos
dc.description.fil
Fil: Holschneider, Daniel P.. University of California at Los Angeles; Estados Unidos
dc.description.fil
Fil: Guo, Yumei. University of California at Los Angeles; Estados Unidos
dc.description.fil
Fil: Wang, Zhuo. University of California at Los Angeles; Estados Unidos
dc.description.fil
Fil: Roch, Margareth. University of California at Los Angeles; Estados Unidos
dc.description.fil
Fil: Scremin, Oscar Umberto. University of California at Los Angeles; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
dc.journal.title
Journal of Neurotrauma
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1089/neu.2012.2657
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://online.liebertpub.com/doi/abs/10.1089/neu.2012.2657
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